The Female(?) Athlete Triad - Part I/III: How An Evolutionary Advantage Can Turn Its Ugly Face On Both Sexes!

The cover of the Vogue is usually not the place to turn to, if you are looking for role-models, but let's be honest: Do you believe Hope Solo or Serena Williams suffer from amenorrhea or their fellow Olympian Brian Lochte from low testosterone? I don't think so. So, there must be something "real" athletes do that way too many weekend warriors, who are in it, often to look just like their stars don't do - and in this multi-part SuppVersity Special, we are going to figure out what this may be.

I guess some of you will already have believed that I had forgotten about the requested and promised article on the "Female Athlete Triad". As you can easily see, this is not the case and still, I must admit that it will take another week until I will eventually have make good on my promise, as this is only the first part of a multi-part feature.

The main reason I decided to split things up is that I did not want you to simply skip on the fundamental information you will get today and fast forward to the potential solutions to the problem, I will present in the next installment.

After all, the idea of the SuppVersity is not to present cookie-cutter guru advice that may or may not work for you, but rather to put you into a position, where you do at least understand, at best have the skills to question, modify and tweak any exemplary "plans of attack" I will be outlining in upcoming the second part of this series... and if my past efforts to provide you with a basic understanding of your own metabolism have not totally failed, I would suspect that many of you will be able to come up with their own preliminary conclusions after reading this lengthy, but as I hope informative and not overtly complicated first part of the series.

"Female athlete triad:" How the problems start with a false label, already

But my bones are still strong! Specifically the inclusion of osteoporosis as an obligatory criteria for the diagnosis of the female athlete triad is nonsensical and was repeatedly criticized (e.g. Kahn. 2002), as it excludes a large, if not the major part of women (and men) who suffer from a syndrome the prevalence and consequences of which are thus largely underestimated. Moreover, in weight bearing sports, for example the load alone will counter the occurrence of osteoporosis, while other consequences like musculoskeletal injuries will be more prevalent.

So, let's initially take a look at what we are actually talking about here. The phenomenon itself is often somewhat misleadingly labeled as the "female athlete triad" (FAT; or AT w/out the sex-specificity), a term which falsely implies that it was sex-specific and men were immune to it and, what may be even worse, that it would be quite easy to diagnose as it comprises a "triad" of

• low energy availability / disordered eating
• amenorrhea, and
• osteoporosis

Unfortunately, things are much more complex than that and when an athletes health has been deteriorated so much, already, that amenorrhea (or very low testosterone in men) and osteoporosis are already showing their ugly faces, reversing the low energy availability and / or disordered eating, which usually goes hand in hand with months of overtraining, may be enough to keep the status quo, but won't reverse the amenorrhea and the underyling hormonal imbalance.

How prevalent is this misery?

Even if we don't extend our definition to include overall exhaustion and stagnating performance on the "harmless" and "heart disease" and "sudden cardiac death" on the other "life-threatening" end of the continuum, but simply include low testosterone levels and minor menstrual irregularities into our definition of AT (athlete triad), the answer to the above question is "It is rampant!" So rampant in fact that Luigi Di Florence chose the title "Does the high performance athlete need hormone replacement?" for a talk he held at a recent conference. In the respective abstract (a paper has not yet been published), he states:

Figure 1: Moroccan Sahraoui women still have a very different beauty-ideal than Western women. According to the data Rgubi et al. collected in 2006, their female beauty-ideal is heavier than the "health ideal". There is however a clear trend towards a "westernization" among the younger generation (data based on Rguibi. Now, tell me, where would you place yourself, your beauty-ideal and your health ideal on the graphic in the upper left hand of this figure?

"Exercise per se is associated to the release of different hormones: acute exercise stimulates an acute hormones secretion (e.g. catecholamines, growth hormone, CRH-ACTH-cortisol, testosterone) while chronic exercise (training) is able to modify hormones secretion at rest and their activation during acute exercise. [...] besides symptomatic classical diseases or conditions that may reduce/alter the qualitative/quantitative hormones secretion, serious clinical concerns exist for asymptomatic endocrine hypo-function (e.g. sub-clinical hypogonadism, growth hormone deficit and hypothyroidism), particularly in adult athletes. For example, in master athletes we observed an high prevalence of undiagnosed severe (12%) and mild (18%) hypo-testosteronemia frequently in the absence of clinical symptoms. [...] Unfortunately, few studies evaluated the prevalence of reduced hormones secretion in athletes and the concept of adapted hormone replacement in high competitive athletes." (Di Luigi. 2012; my emphases)

The absence of a clearcut definition of "the female athlete triad", the ignorance towards the existence of corresponding problems in male athletes (of all age groups!) and the vast differences within different study populations makes it very difficult to quantify, how many men and women actually suffer from AT. The little data we have is obviously sex-specific and of rather qualitative nature, as the following citation from Hobart 2000 goes to show you:

Although the exact prevalence of the female athlete triad is unknown, studies have reported disordered eating behavior in 15 to 62 percent of female college athletes. Amenorrhea occurs in 3.4 to 66 percent of female athletes, compared with only 2 to 5 percent of women in the general population. (Hobart. 2000)

If we take the latest NCAA numbers as a baseline (191,131 female athletes in the year 2011) and multiply them by 2x to include those lonesome gymrats and crossfitters out there who are often even more likely to overdo it than their co-ed peers who usually work with a more or less qualified coach, of whom you would expect that he or she is able to call a halt before it is too late, we are talking about ~13,000-252,000 young women and an undisclosed number of young men, here!

"Sh..Sh.. let's not talk about it!"

Pah, that's all not problematic! Really? A 2002 study from the Bell State University found that aside from the menstrual irregularity, which have been reported by 31% of the athletes not using oral contraceptives, both, muscle and bone injuries were rampant: 65.9% and 34.3%, in the aesthetic versus endurance and team/anaerobic sports, respectively. (data based on Beals. 2002)

Against that background it is almost careless, how little this topic is talked about - especially among athletes and fitness junkies! No wonder that only 10% of the 191 female exercisers (age 18-40 yr), engaging in ≥2 hr/wk of strenuous activity, Miller et al. questioned for their 2012 study on "the knowledge, attitudes, and behaviors of regularly exercising adult women in Australia", could name the initially mentioned three components of the female athlete triad:.

"Regardless of reported history of stress fracture, 45% of the respondents did not think that amenorrhea (absence of menses for ≥3 months) could affect bone health, and 22% of those involved in lean-build sports would do nothing if experiencing amenorrhea (vs. 3.2% in non-lean-build sports, p = .005)." (Miller. 2012; my emphases)

This lack of knowledge and - in parts - even downright ignorance towards the problem certainly raises the question:

"How do I actually realize I am about to develop the (female) athlete triad (AT)?"

I guess, we can derive a (not the!) answer to this question if we take a closer look at an overview of the etiology that has been part of a 2002 analysis by Melinda M. Manore from the Department of Nutrition and Food Management at the Oregon State University in Corvallis, Oregon, USA (see figure 2).

Figure 2: Etiology of the (female) athlete syndrome (and related pathologies) and signs you have to observe, in oder not to to realize what you have been doing when the potentially life-threatening long-term conequences, i.e. bone loss, cardiovascular disease and hardly reversible issues with reproductive function are showing (inspired by Manore. 2002)

I pimped the original graphic with a couple of remarks that should make one thing pretty obvious: At the very moment, when the "classic" features become obvious, it's actually already to late. The best you can hope for, when your menses start to disappear is that neither your cognitive abilities, nor your cardiovascular or bone health are not yet compromised, as well.

There is hope - even after the horse has bolted

"Men can't be anorexic?!" False! According to the latest data from the South Carolina Department of Mental Health there are currently 1,000,000 male US citizens suffering from eating disorders. Their estimated stake among anorexics and bulemics is between 10-15%. Among adolescents, anorexia is the 3rd most common chronic illness, and many of it's physical features are identical to those of the "female" athlete triad - not the least due to the fact that excessive exercise is often part of the pathology. The boundaries between them are fluid. The mortality rate associated with anorexia nervosa is 12x higher than the death rate of ALL causes of death: 5 – 10% of anorexics die within 10 years after contracting the disease; 18-20% of anorexics will be dead after 20 years and only 30 – 40% ever fully recover.

The good news is that our bodies (male and female) are self-repairing machines, evolutionary designed to take beating after beating - esp. if those "beatings" resemble periods of famine. From studies in anorexic men(!) and women we know that many of the pathological features of self-cannibalism (this, and nothing else is what your body is doing, when you constantly deprive it of an adequate supply of energy, as it is the case in the accute phases of the athlete triad) are reversible.

Mont et al. who have been following 31 severely underweight anorexic adolescents with body mass indexes of 15.2 +/- 2 kg/m², sinus bradycardia (=abnormally slow heart beat), decreased left ventricular mass, and diminished thickness of cardiac walls in 35%, 93% and 70%, respectively, report for example:

"After refeeding, a significant decrease in QT interval (p <.05) and QT dispersion (p <.01) was observed. Echocardiograms showed an increase in cardiac diameters (p <.01), left ventricular mass (p <.001), and cardiac output (p <.001). There was also an improvement in the exercise capacity (p <.05) and a normalization of the heart rate and heart rate variability (p <.05)." (Mont. 2012)

Allegedly, few athletes will maneuver themselves into a situation, where they are actually so weak that they can barely walk (which is unfortunately the case for way too many young anorexic patients), their susceptibility to sudden cardiac death and other CVD-related diseases is probably even higher, due to the exercise induced chronic overload of their cardiovascular system.

With the athlete's triad an evolutionary advantage is turning is turning against us

Athlete or not, even these severe physical abnormalities usually disappear with adequate rest, lots of patience and, most importantly, a progressive increase in energy intake (the increases in lean mass, i.e. muscle, organ and bone!, wants to be fed and the the metabolic switch from "energy save" to "normal" mode will increase the energetic demands even more). In fact, even in severely anorexic patients, where most of these pathologies are more severe than in athletes, renal abnormalities (Boag. 1985), atrophy of the bone marrow (Steinberg. 1987; Orlandi. 2000), cognitive impairment (Mikos. 2008) and most of the other functions that are related to survival (not reproduction!) usually recover with adequate energy intake, alone.

Without the evolutionary preserved, catecholamine and glucocorticoid driven "hunger high" our ancestors needed to keep going until they finally found something to eat, neither anorexia (AN), nor the athlete triad (AT) would "work".

The fact that many, if not most of the patients feel that the latter would not help and they would "just become fat", has both psychological, as well as physiological roots, which are related to (a) a distorted body image (which has by the way nothing to do with "being crazy", let alone "dumb" or "stupid") and (b) the loss of the "hunger high", which has previously been masking all the ailments and the total exhaustion and will begin to fade after only 1-2 days of sufficient energy supply and rest.

For many, it does in fact feel, as if they had just been hit by a truck, but in fact very truck has rolling right over them for years now and the person behind the steering wheel, was nobody else than the patient him-/herself.

Without the hilarious amounts of glucocorticoids (cortisol) and excitatory neurotransmitters their bodies seize producing, now that they are no longer necessary to keep the brain from dying a hypoglycemic death and the patients able and motivated to "seek for food" (another evolutionary preserved mechanism, by the way), all the weight of years of over-training and under-eating hits them all at once. In conjunction with the unwanted, but inevitable weight gain, of which Golden et al. state that it comes - specifically in this early phase - almost exclusively from increases in body water, organ, bone and muscle mass (Golden. 2004), this often triggers a relapse into the old "cosy" stress pattern of under-eating and over-exercising. And what's really nasty, here, is that this will provide (felt) "relief" within days, if not hours and via the exact same mechanism that has kept the patients going (and later alive!) over the past months and years: HUNGER (not workout) STRESS!

Not BMI, not fat, not exercise, but simply a constant state of energy deprivation is the culprit

Since we are all aware that weight gain does not happen over night, but the aforementioned perceived aggravation of fatigue can, it should be obvious that neither a low body weight, let alone the amount of body fat a person, man or women, is carrying on his/her frame (scientists refer to this as the "body composition hypothesis), nor the exercise induced stress ("stress hypothesis"), of which I have just outlined that it is a necessary and life-saving reaction to starvation, are at the root of the poblem. The true causative factor is (at least according to the current paradigm) the lack of a sufficient and constant supply of readily available energy (we are not talking about leafy greens and chicken breast, here!).

Evidence against the "body composition" hypothesis: After a surgical reduction of the stomach volume even obese women can develop amenorrhea

The most convincing evidence for the so-called "energy availability hypothesis", specifically in view of the hormonal aspects of the athlete triad, comes from a 1999 study on the short- and long-term outcomes of a surgical reduction of the stomach volume in severely obese women. Due to their artificially induced physical inability to consume adequate amounts of energy, these women, who were even after they had lost massive amounts of body weight still obese (BMI > 35!) developed amenorrhea (Di Carlo. 1999).

In this context, Anne B. Loucks who worked in the Department of Biological Sciences of the Ohio University in Athens, back in 2005, points out:

"Interest in the body composition hypothesis was rejuvenated several years ago by the discovery of leptin. Because leptin is secreted by adipose tissue cells, it was originally thought to signal information about the size of body fat stores. Rapid and profound declines in leptin were soon observed in response to fasting and dietary restriction, how-ever, and similarly extreme increases were observed in response to overfeeding and refeeding after energy restriction, all before changes in adiposity could occur. These observa-tions led to the revised hypothesis that leptin actually signals information about dietary energy intake. Since then, however, we have shown that the level and diurnal rhythm of leptin actually depend on energy availability (defined as dietary energy intake minus exercise energy expenditure) and that exercise itself has no suppressive effect on leptin beyond the impact of its energy cost on energy availability." (Loucks. 2005; my emphases)

In other words, the same hypothesis that initially pointed towards the amount of leptin secreting adipose tissue as a regulator of the hormonal balance in amenorrhetic women (the "body composition hypothesis"), does now, that it appears clear that energy availability and not body fat stores determine the secretion of leptin, clearly indicate that body fatness is a subordinate (as being the consequence of constant dieting) indicator of a persons susceptibility to suffer from hormonal imbalances, at best.

For similar reasons, the "stress hypothesis" which points with a finger at the exercise induced increases in cortisol is bullocks, as well. After all, those increases in cortisol and catecholamine expression are - just like low leptin levels - a necessary and healthy adaptation to the absence of a constant and adequate supply of energy. Without the glucocorticoids (just in case you still don't get it: "gluco" as in "glucose" <= the stuff everybody is scared about these days) no athlete or anorexic patient would be able to maintain normal blood glucose  - without any cortisol, they would simply die.

Evidence for the "energy availability hypothesis"

Figure 4: 24h-LH profile in healthy women after 5 days of normal (top) as well as calorically restricted (-33, -66, -87%) nutrient intake (arrows indicate meals, the black bar indicates sleep).

In fact, Loucks and her team at the Ohio University have conducted a whole series of studies the results of which support the "energy availability hypothesis" and I want to conclude this first part of the two-part series with the one study that segues directly into part II of this series, which will zone in on the the problem of persistent hormonal imbalances and their dietary and behavioral underpinnings.

In this regard, the profound disturbances in the pulsatile release of luteinizing hormone (LH) from the gonadotroph cells in the anterior pituitary gland, Loucks et al. observed after only 5 days of

• 33% - lower LH amplitude
• 66% - increased amplitude decreased frequency
• 77% - further decrease in frequency + increase in amplitude

calorie restriction, the scientists observed "regardless of whether energy availability was reduced by dietary restriction alone or by exercise energy expenditure alone" (Loucks. 1998) set the scene for a discussion that will be relevant for both, male and female physical culturists.

Don't forget to come back next week for part II!

In other words, if you want more about the role of the thyroid gland, of adiponectin and insulin sensitivity, of ghrelin and growth hormone, of insulin and IGF-1 and the circadian clock and intermittent fasting in the etiology of the athlete triad and which tweaks to your nutrition, exercise and supplementation regimen can help you not end up in a viscous circle that will not just hamper your perfomance, but compromise your physique and physical and psychological well-being, come back next Sunday for part II of the SuppVersity Athlete's Triad Special.

References

• Argente J, Caballo N, Barrios V, Muñoz MT, Pozo J, Chowen JA, Morandé G, Hernández M. Multiple endocrine abnormalities of the growth hormone and insulin-like growth factor axis in patients with anorexia nervosa: effect of short- and long-term weight recuperation. J Clin Endocrinol Metab. 1997 Jul;82(7):2084-92.
• Beals KA, Manore MM. Disorders of the female athlete triad among collegiate athletes. Int J Sport Nutr Exerc Metab. 2002 Sep;12(3):281-93. 
• Boag F, Weerakoon J, Ginsburg J, Havard CW, Dandona P. Diminished creatinine clearance in anorexia nervosa: reversal with weight gain. J Clin Pathol. 1985 Jan;38(1):60-3.
• Di Carlo C, Palomba S, De Fazio M, Gianturco M, Armellino M, Nappi C. Hypogonadotropic hypogonadism in obese women after biliopancreatic diversion. Fertil Steril. 1999 Nov;72(5):905-9.
• Di Luigi L. Does the high performance athlete need hormone replacement? Endocrine Abstracts. 2012; 29: 35.1 
• Figueiro MG, Plitnick B, Rea MS. Light Modulates Leptin and Ghrelin in Sleep-Restricted Adults. International Journal of Endocrinology. 2012, Article ID 530726.
• Golden NH, Meyer W. Nutritional rehabilitation of anorexia nervosa. Goals and dangers. Int J Adolesc Med Health. 2004 Apr-Jun;16(2):131-44.
• Hernández M, Argente J, Navarro A, Caballo N, Barrios V, Hervás F, Polanco I. Growth in malnutrition related to gastrointestinal diseases: coeliac disease. Horm Res. 1992;38 Suppl 1:79-84.
• Hobart J, Smucker D. The Female Athlete Triad. Fam Physician 2000; 61:3357-64,3367. 
• Khan KM, Liu-Ambrose T, Sran MM, Ashe MC, Donaldson MG, Wark JD. New criteria for female athlete triad syndrome? As osteoporosis is rare, should osteopenia be among the criteria for defining the female athlete triad syndrome? Br J Sports Med. 2002 Feb;36(1):10-3. 
• Leibel RL, Rosenbaum M, Hirsch J. Changes in energy expenditure resulting from altered body weight. N Engl J Med. 1995 Mar 9;332(10):621-8. Erratum in: N Engl J Med 1995 Aug 10;333(6):399.
• Loucks AB, Verdun M, Heath EM. Low energy availability, not stress of exercise, alters LH pulsatility in exercising women. J Appl Physiol. 1998 Jan;84(1):37-46.
• Loucks AB. Energy availability, not body fatness, regulates reproductive function in women. Exerc Sport Sci Rev. 2003 Jul;31(3):144-8.
• Lu M, Tang Q, Olefsky JM, Mellon PL, Webster NJ. Adiponectin activates adenosine monophosphate-activated protein kinase and decreases luteinizing hormone secretion in LbetaT2 gonadotropes. Mol Endocrinol. 2008 Mar;22(3):760-71. Epub 2007 Nov 15.
• Manore MM. Dietary recommendations and athletic menstrual dysfunction. Sports Med. 2002;32(14):887-901. 
• Mikos AE, McDowell BD, Moser DJ, Bayless JD, Bowers WA, Andersen AE, Paulsen JS. Stability of neuropsychological performance in anorexia nervosa. Ann Clin Psychiatry. 2008 Jan-Mar;20(1):9-13.
• Miller SM, Kukuljan S, Turner AI, van der Pligt P, Ducher G. Energy deficiency, menstrual disturbances, and low bone mass: what do exercising Australian women know about the female athlete triad? Int J Sport Nutr Exerc Metab. 2012 Apr;22(2):131-8.  
• Modan-Moses D, Stein D, Pariente C, Yaroslavsky A, Ram A, Faigin M, Loewenthal R, Yissachar E, Hemi R, Kanety H. Modulation of adiponectin and leptin during refeeding of female anorexia nervosa patients. J Clin Endocrinol Metab. 2007 May;92(5):1843-7. Epub 2007 Feb 27.
• Mont L, Castro J, Herreros B, Paré C, Azqueta M, Magriña J, Puig J, Toro J, Brugada J. Reversibility of cardiac abnormalities in adolescents with anorexia nervosa after weight recovery. J Am Acad Child Adolesc Psychiatry. 2003 Jul;42(7):808-13.
• NCAA® Sports Sponsorship and Participation Rates Report • 1981-82 – 2010-11.  
• Orlandi E, Boselli P, Covezzi R, Bonaccorsi G, Guaraldi GP. Reversal of bone marrow hypoplasia in anorexia nervosa: case report. Int J Eat Disord. 2000 May;27(4):480-2.
• Otto B, Cuntz U, Fruehauf E, Wawarta R, Folwaczny C, Riepl RL, Heiman ML, Lehnert P, Fichter M, Tschöp M. Weight gain decreases elevated plasma ghrelin concentrations of patients with anorexia nervosa. Eur J Endocrinol. 2001 Nov;145(5):669-73.
• Rguibi M, Belahsen R. Body size preferences and sociocultural influences on attitudes towards obesity among Moroccan Sahraoui women. Body Image. 2006 Dec;3(4):395-400. Epub 2006 Sep 7. 
• Scacchi M, Ida Pincelli A, Cavagnini F. Nutritional status in the neuroendocrine control of growth hormone secretion: the model of anorexia nervosa. Front Neuroendocrinol. 2003 Jul;24(3):200-24.
• Scheid JL, De Souza MJ. Menstrual irregularities and energy deficiency in physically active women: the role of ghrelin, PYY and adipocytokines. Med Sport Sci. 2010;55:82-102.
• Schtscherbyna A, Barreto T, de Oliveira FP; Luiz RR, de Abreu Soares RR, Gonçalves Ribeiro B. Age of onset training but not body composition is crucial in menstrual dysfunction in adolescent competitive swimmers. Rev Bras Med Esport. May/June 2012; 18(3).
• Steinberg SE, Nasraway S, Peterson L. Reversal of severe serous atrophy of the bone marrow in anorexia nervosa. JPEN J Parenter Enteral Nutr. 1987 Jul-Aug;11(4):422-3.
• Sundgot-Borgen J. [Physical activity and reproductive health]. Tidsskr Nor Laegeforen. 2000 Nov 20;120(28):3447-51.
• Williams NI, Helmreich DL, Parfitt DB, Caston-Balderrama A, Cameron JL. Evidence for a causal role of low energy availability in the induction of menstrual cycle disturbances during strenuous exercise training. J Clin Endocrinol Metab. 2001 Nov;86(11):5184-93.

Adelfo Cerame Road to Wheelchair Championships: Six Diet Tips to (Six-)Pack on Lean Mass Between Two Shows

Image 1: The drafter, he is, Adelfo is probably enjoying the increased workload inside and outside of the gym.

Time is, and I am probably not writing this for the first time, flying by, these days. It is yet another Thursday and once more, I am about as intrigued about Adelfo's progress in the past seven days, as you (probably?) are. We have been talking quite a lot, actually, but not so much about his own regimen, as about other stuff, such as the first boydbuilding seminar, Adelfo attended as an official Myotropics Physique athlete. Kind of amazing how things are taking off for him and I am truly happy that all the hard work he has and still is putting not only in his physique, but also in his education is starting to pay off. That being said, you are lucky that he has found some time to compile his weekly blogposts in-between his homework assignments at school, his training and the marketing events for Myotropics, who are just about to release their first product, Physique 2.0. So, let's get right to the grind, as Adelfo would probably say...

Three weeks of training: Time to (re-)evaluate the plan

Six weeks, since the Florida show and another 11 weeks to go until my next show, the USA's in New Orleans. In the past three weeks I have really stepped up my training. Not just because I changed my plan and incorporated different training techniques (cf. "Adelfo Cerame's Hypertrophy-EDT-5x5 Crossover Regimen") but first and foremost due to the application of different training techniques such as modified times under tension, increased workloads in my EDT regimen and the higher volume training in the hypertrophy part of my training split.

While I stuck to the EDT/5x5 part of the split in the first two weeks after the Florida Nationals, I am now on my first week of the hypertrophy + 5x5 combination and will stick to it for the next two weeks, thusly alternating the EDT/5x5 and the 5x5/hypertrophy split, every other week. Even that is a departure from the original weekly rotation, but after the first  round on the hypertrophy/5x5 split this week, I am actually considering to keep training this way for the majority of my prep, just throwing in the the EDT sessions every other three weeks or so.

Figure 1: Current hypertrophy + 5x5 routine (Adelfo Cerame Jr. 2012)

As you can see, I vary my rep schemes depending on the exercises I do; I feel that my muscles need more stimulation and time under tension during certain exercises compared to others. Therefore I vary the reps between 8-10 and 10-12 reps per set and go down into the 6-8 rep range, whenever I feel that the exercise is particularly suited to go real heavy. That being said, I am not even trying to lift moderate, let alone light weights, I still try to lift as heavy as I can, but pick weights which will allow me to hit the prescribed amount of reps.

A note on setting your rep ranges right: With my 5x5 routine, I’ve learned in the past that 5x5 regimen work particularly well with compound movements; and while I have tried doing cable flys, triceps pulls and the like with five or even less reps in the past, you really don’t get much out of those exercises in the lower rep ranges. When you are training on a higher volume hypertrophy split, on the other hand, you do obviously want to incorporate more of these isolation movements into your routine, where - as Dr. Andro's hypertrophy routine exemplified - you will then train at the other end of the hypertrophy range, incorporating the occasional real high rep work (15-25 reps) as a means to really exhaust the muscle.

So far, I am very satisfied with my training regimen and very pleased with the way my training has been going. I feel that with these alternate splits of heavy lifting combined with hypertrophy training, I’ll be able to gain a little bit more muscle within the small time-window I have before I gradually start to taper down my calories within the next week or so…

Apropos caloric intake: A brief lesson in tapering up and down your food intake

I mentioned in previous blogposts here at the SuppVersity that I would be gradually increasing my calories to take full advantage of the small window of opportunity I have before I really have to start dialing it in again for the USA’s in New Orleans. Fortunately I did not ruin my physique after my Florida show (for a breakdown on how Adelfo did that, click here), and was able to maintain a very low body fat percentage. That gave me the luxury to play around and try to increase calories (rather than cutting them back again, right away), while still trying to burn fat or at least keep fat gains to a minimum.

Adelfo Cerame's In-Between the Shows Mini-Bulking Guide - Physique athlete, bodybuilder or just someone who "wants to look good naked", I guess at least the male part of the fitness community, will (and the female should) be faced with this question at some time: "How do I manage my energy intake to maximize my lean muscle gains and minimize fat gains?" As Dr. Andro would probably say it, "I don't have the hubris to tell you that I knew the answer to this question", but I still feel that some of the things I have learned in the past may well guide you on your way to a more muscular, yet not fattier self:

1. It’s always smart to slowly increase calories so your body has time to adjust. For myself, I usually prefer a 200-300kcal increase/week, which would be a 50-75g increase in carbohydrates; which is the macronutrient that I usually adjust when I make increases or decreases. The reasoning behind this strategy is that I like to keep my protein intake fairly constant and my fats moderate to high, depending if I’m cutting or trying to build lean mass; I have yet learned from past (low) fat mistakes, and will never go lower than 50g/day with my fats.
    
2. Adding carbs gradually here and there is a good way to slowly increase calories, like I mentioned above, you manage your caloric surplus by modulating your carb intake and in order not to overwhelm your body, you better make sure to go slowly, in order to make sure that you do not pass over your individual threshold (I emphasize "individual" here, because the latter will not only vary from person to person, but is also susceptible to influences from previous diets, your current training regimen, your stress levels and, obviously, your current body fat levels and overall health). Personally, I have found that 50-60g of carbohydrates immediately after my workouts (shakes + fast carbs) and another 100g in the vicinity of the workout (most of them as starchy carbs in my post-workout meal) appear to be my magic numbers.
    
3. When you do intermittent fasting, your body is tuned to run on fats for fuel so, I that I don't see any reason to ingest large amounts of carbs before I work out or during my rest days. I thusly ingest the lion's share of my weekly carbohydrate intake after my workouts. With carbohydrates being the macronutrient by which I adapt my total caloric intake, this does also mean that I have a built in "high calorie / low calorie cycle", with currently 180g protein/ 200g carbs/ 55g fat on my workout days; 50g immediate following my workout and 100g in the real food meal thereafter. The rest of the 50g are trace carbs from my raw milk, cottage cheese and, not to forget, my Physique 2.0 meal supplement shake, I ingest before my workouts and pre-bed to take advantage of the protein anabolic effects of the slow releasing total milk proteins and the increased fatty acid oxidation from the WM HDP in it's carbohydrate fraction.
    
4. Never surpass your individual carb threshold, to monetize on the muscle building performance enhancing effects of carbs, without compromising your physique. For me 200g of carbohydrates are (currently) the sweet spot, with a maximum of 100g of carbs (mixture of slow and fast digesting) in my post workout meal being the upper limit on a "per serving" basis. If you stick to clean foods and refrain from the artificial flavored junk you buy on every corner, it is actually not that difficult to distinguish between being really full and satisfied and having surpassed the threshold of reasonable glycogen replenishment.
    
5. Judge your diet by the way you look in the morning, and don't get fooled by the intermediate bloat right after a meal. Specifically if you are eating whole maximally satiating foods with a high volume, that alone will make your stomach stick out. Add to that any intermediate bloat in response to the temporary fluid loss and replenishment during and after your workout and you know why the same waist that looked disgustingly protruded after your PWO meal is back to its normal size on the morning thereafter.
    

6. 

   Image 2: If you don't acknowledge that bodybuilding is an art, you will never make it to the stage.

   Don't calculate calories as if your body knew what a "calorie" is. I know that it's difficult and even I am guilty of it from time to time, but think about it, can you say exactly how many meters you will be able to make with one tankful of gas? I don't think so and that despite the fact that you car is a much less sophisticated machine than your body. Just as you won't get as far at 130mph as you would get with 30mph, your bodies caloric expenditure depends largely on your current metabolic rate, which in turn is influence by your weight status, our prior diet, your endocrine health, etc.
   
   This is why you should never start out from any sort of calculated baseline, but just build on what you are eating now and go from there re-evaluating your diet on a weekly (not a daily) base), closely monitoring the way you look, feel and perform (weekly progress pics and a measuring type for your waist, are a must, scales - even those showing you random bf% are obsolete).

I guess, some of you may have expected some sort of formula or "magic number" that will work for everyone and will now be disappointed that you still "don't know how much to eat" - so if that's you, you do at least know why all your efforts to build a better physique have failed. If you don't acknowledge that bodybuilding is at least as much an art, as it is a science, you better attend Dr. Andro's physics classes, instead of studying his bogposts, here at the SuppVersity.

After a few conversations with Adel, ah.. I mean Dr. Andro ;-) I decided to slowly build up to caloric intake in the 2000-2100kcal range and see how this affects my body. Having hit the mark this week with seeing hardly any negative and a lot of positive side effects, I am now at the point to decide whether

• to stick to where I am and try to build some more muscle mass on what I suspect would be a maintenance level,
• to kick it up a notch and try go for a "hardcore mini bulk" trying to build as much muscle as possible even if this goes hand in hand with a minor increase in body fat levels, or
• to start cutting back again and hope that - just as with my last prep - the gradual and slow decrease in caloric will facilitate a minimal gain in muscle mass while I am still gradually losing body fat

Take a look at where I am now. What would you do? Put an end to the "mini-bulk" I am on right now, keep rolling, increase or decrease the energy intake?

Figure 1: Adelfo Cerame Jr after 2+1/2-weeks of "mini-bulking" before the USA Wheelchair Championships.

I guess I have already put on a little more muscle mass, or at least, I have gotten a lot fuller over these past weeks - at the expense of some water retention, yeah... specifically in my lower abs. But I will take care of that once I start dialing in my calories again. So, what do you think SuppVersity Readers? Keep pushing it another three weeks?

Protein Intake & Muscle Catabolism: Fasting Gnaws on Your Muscle Tissue and Abundance Causes Wastefulness

How much of the protein you can eat and how much of it you need two keep the status quo are very different questions.

Don't worry, this article is not about the notorious "Anabolic Barndoor" or the purported magic of "nutrient timing" and post.workout supplements. The thing I want to discuss in today's SuppVersity article is of a more general nature and revolves around the upregulation of the ubiquinase enzymes and consequent proteolysis (=catabolims) of skeletal muscle tissue ... or if you want to use my buddy Carl Lanore's term: "The loss of metabolic currency" we all know you better avoid at all costs, if you care about aging healthily. 

You can learn more about protein intake at the SuppVersity

Are You Protein Wheysting?

Cod protein for recovery

Protein requ. of athletes

High EAA protein for fat loss

Fast vs. slow protein

Too much ado about protein?

What we are going to deal with today is protein breakdown, or the purported general anticatabolic effect of high protein diets. To this ends, we will be taking a closer look at the ubiquitin proteasome system (UPS) response to constant energy deficits (ED) at varied dietary protein intakes before and after the consumption of a high protein meal replacement. An issue, by the way, that was also addressed in a paper that has been published a couple of days ago in the peer-reviewed scientific journal FASEB (Carbone. 2013).

No, this is not a deja vue! You've actually read about the same experiment, yet a different portion of the results back in June, in one of my previous articles on optimal protein intake / supplementation | read more 

In said paper by scientists from the School of Health Sciences at the Eastern Michigan University, the Nutrition Division at the U.S. Army Research Institute of Environmental Medicine, the Human Nutrition Research Center that's located at the U.S. Department of Agriculture, and the School of Medicine and Health Sciences at the University of North Dakota thirty-nine young, fit and healthy adult volunteers, who were caged in a metabolic ward, were randomized to one out of three groups with different baseline protein intakes:

• 0.8g/kg body weight of protein (RDA)
• 1.6g/kg body weight (2 -RDA), or 
• 2.4g/kg body weight (3 -RDA)

The participants, 32 men and 7 women, had to be between the ages of 18 and 42 yr and of stable weight ( 2 kg for a period of 2 mo), to have a body mass index (BMI) between 22 and 29 kg/m²,
and to be physically fit [peak oxygen intake (Vo2peak) 40–60 ml/(kg ·min)].

The subjects followed the prescribed dietary protocol for a whole month (31 days), went into a tightly controlled 10-day weight maintenance phase and started fasting for 21 days, immediately thereafter (Note: To keep the protein intake stable, the dietitians who planned and prepared the meals for all study participants had to prepare meals with a significantly higher relative protein content),

In this study: 30% energy restriction +10% physical activity = "fasting"

Just to avoid any confusions: The above, i.e. a 30% reduction in energy intake and a 10% increase in physical activity, is what John W. Carbone and his colleagues talk about, when they use the word "fasting". It does not mean that the subjects have been sitting in one of those tents, where you can actually measure the energy expenditure for 21-days eating nothing, but their finger and toe nails.

An important note on the accuracy of calculated: While Carbone et al. state that their -30% intake, +10% expenditure protocol will produce an energy deficit of 40%, I'd hope that you as seasoned SuppVersity students see through the futility of calculations like these and let go off figures that signify a degree of exactness that's simply not there.

In view of the fact that the term "fast" is contemporarily used to designate "diets" that are really low in energy (up to ZERO calories, intermittently), I suspect I should also mention that I personally would call the last 21 days of the study the "diet" not "fasting" phase.I mean, 30% reduced energy intake and +10% physical activity? We all know that the health and physique 90% of our fellow men and women would benefit from this regimen.

Muscle biopsies and enzyme expressions

The scientists took muscle biopsies before (fasted) and 2h after (fed) the ingestion of "a commercial nutrition supplement (Boost; Nestlé HealthCare Nutrition, Florham Park, NJ, USA)" with a total energy content of 480 kcal and 20 g of protein to assess the degree of intracellular proteolysis on day 10, i.e. right before the "fast", and day 31, i.e. right after the "fast", of which Carbone et al. write that it was based on individualized menus that were administered under supervision, to ensure compliance.

"To maintain fitness, the volunteers performed resistance type physical activity 3 d/wk, and daily endurance-type exercise, at levels comparable to those they had reported in their prestudy activity logs. To minimize the potential that an unaccustomed training stimulus would influence skeletal muscle outcomes and to ensure accuracy, research personnel closely controlled and monitored the intensity and volume of physical activity. For resistance-type exercise, the volunteers performed 1 single-joint movement per major muscle group (3 sets of 15 repetitions), using workloads determined during the prestudy period. The intensity of the endurance-type activity (40 – 60% VO2peak) was based on prestudy measurements, and verified by indirect calorimetry (ParvoMedics) and the corresponding heart rate during familiarization trials conducted before the study, and by the heart rate reserve-method throughout the interventio." (Carbone. 2013)

The 10% increase in physical activity was achieved by an increase in the length of the daily endurance training sessions that would accommodate for the corresponding increase in energy expenditure

Figure 1: Changes in lean body mass and fat mass (kg) that occured during the 21-days on 40% energy restricted diets with varying amounts of dietary protein in it (based on Pasiakos. 2013)

As you can see in Figure 1, which is based on results the researchers presented in a previous publication that was likewise discussed, here at the SuppVersity, this intervention was not without consequences on the body and fat mass of the study participants who lost on average 3.2 ± 0.2 kg body mass, but at very different lean:fat-mass ratio (learn more).

What's the more important "-bolism": Cata- or ana-bolism?

In contrast to their previous paper that focused exclusively on the increase in muscle protein synthesis, this "follow up"* discards the influx of dietary protein into the muscle of the subjects and focuses on the proteolytic enzymatic response to the diet  (*I assume both were filed at the same time, but the one in FASEB was published ahead of print, while the one at hand did not).

Figure 2: Enzymatic activities for 26S 1(A), 26S 2(B), 26S 5(C), and caspase-3 (D). Open bars, weight maintenance; solid bars, energy restriction.

Put differently, instead of asking the likewise important question: "What's more anabolic?" that was already answered in the paper by Pasiakos et al. (read more). Carbone et al. focus on the similarly or even more important question: "What's more catabolic?" - with a quite intriguing outcome, if I may say.

I mean, you would expect that the activity of the catabolic enzymes would vary depending on the protein content of the diets, wouldn't you? No? Well, maybe you did expect that the response to the 20g protein shake the subjects consumed would have an effect on their expression (black bars in Figure 2)?

You didn't? Tthat's awesome, you must be a genius, 'cause nothing of that actually happened. In other words, the expression of proteolytic enzymes did not in any way or form depend on the total amount of protein, the healthy young subjects in the study at hand consumed on a daily basis - once, twice or thrice the RDA of 0.8g/kg body weight.

Take home message #1 -- Your daily total protein intake has no effect on the expression of catabolic enzymes in your musculature. Even your total energy intake has little effect on the expression of catabolic enzymes in your musculature.

And if we are honest, most of us would probably also have expected a much more pronounced difference in these markers of muscle catabolism, when comparing the weight maintenance to the fasting phase (white vs. black bars) - a difference that existed for some yet not all of the ubiquinase enzymes, but was statistically significant for none of them.

Figure 3: mRNA expression of the Ub ligases MuRF1, atrogin-1 and TNF-alpha (Carbone. 2013)

And just in case you find all that not yet surprising enough, I'd suggest you take a parting look at the Murf-1 and atrogin-1 expression in Figure 3 -- what do you see? Correct, Murf-1 and atrogin-1 are the most prominent members of muscle-specific proteases that are highly expressed during muscle atrophy (Gomes. 2001; Witt. 2005); and you are also correct, if you are now scratching your head thinking:

"But how come that both are increased with higher protein intakes?"

Actually you know the answer already. It's after all not just take home message #2 of today's SuppVersity article, but has been addressed in many previous articles on total protein intake and the effects of protein supplementation here at the SuppVersity, as well.

Take home message #2 -- The more protein you eat the more wasteful your body will be (note: this does not mean that the net protein retention does not increase, but it means that you will see diminishing at intakes of thrice the RDA even non-existent returns; cf. "Are you Protein Wheysting?")

So what's left do discuss then? Ah, right, aside from the proteolytic enzymes, the scientists also tested for changes in the expression of TNF-alpha & co and observed that the expression of TNF- mRNA and activation of NF- B1 increased as protein intake exceeded the RDA.

This increase in TNF-alpha and NF-B1 may at first surprise you - TNF [tumor necrosis factor] and consequent NF- B activation are, after all, generally associated with increased muscle proteolysis. If you look back at "take home message #2", however, you'll realize that this, i.e. an increase in muscle proteolysis is exactly what's going on, in the 2x and 3x RDA groups. It is thus also logical that this increase in tumor necrosis factor occurs only in the fed state - a state, when dietary protein is abundantly available.

So what's to be learned on the practical side of things, then? In view of the results of the study at hand, it appears as if we may in fact have overrated the influence of the loss of skeletal muscle protein, i.e. proteolysis, in the past. Compared to the amplitude, or differences between ups and downs of protein synthesis the activity of the proteolytic enzymes is (a) very constant and does (b) depend inversely, but non-linearly on the total amount of protein you eat.

Remember the recent article about the myostatin reducing and thus potentially muscle building effects of low protein diets? | read more

Practically speaking this means that there is a relatively low threshold beyond which the "loss" of protein (=protein not being incorporated into the muscle tissue) keeps increasing, while the storage of protein stagnates. A hypothesis that stands in line with the results of experiments that investigated the differential effects of bolus (=all at once) vs. staggered (=in 4x20g or 8x10g) ingestion of protein supplements (see "Slow or Fast, Bolus or Pulse? Protein Synthetic Response is Identical!" | read more) and the revelation that protein fasting can decrease the expression of myostatin and thus ramp up the capacity for and efficacy of muscular protein storage (see "36% Decrease In Myostatin, With Low Protein (0.1g/kg BW) Diet" | read more).

References:

• Carbone, J. W., Margolis, L. M., McClung, J. P., Cao, J. J., Murphy, N. E., Sauter, E. R., ... & Pasiakos, S. M. (2013). Effects of energy deficit, dietary protein, and feeding on intracellular regulators of skeletal muscle proteolysis. The FASEB Journal, 27(12), 5104-5111.
• Gomes, M. D., Lecker, S. H., Jagoe, R. T., Navon, A., & Goldberg, A. L. (2001). Atrogin-1, a muscle-specific F-box protein highly expressed during muscle atrophy. Proceedings of the National Academy of Sciences, 98(25), 14440-14445.
• Pasiakos SM, Cao JJ, Margolis LM, Sauter ER, Whigham LD, McClung JP, Rood JC, Carbone JW, Combs GF Jr, Young AJ. Effects of high-protein diets on fat-free mass and muscle protein synthesis following weight loss: a randomized controlled trial. FASEB J. 2013 Jun 5. [Epub ahead of print].
• Schakman, O., Dehoux, M., Bouchuari, S., Delaere, S., Lause, P., Decroly, N., ... & Thissen, J. P. (2012). Role of IGF-I and the TNFα/NF-κB pathway in the induction of muscle atrogenes by acute inflammation. American Journal of Physiology-Endocrinology And Metabolism, 303(6), E729-E739.
• Witt, S. H., Granzier, H., Witt, C. C., & Labeit, S. (2005). MURF-1 and MURF-2 target a specific subset of myofibrillar proteins redundantly: towards understanding MURF-dependent muscle ubiquitination. Journal of molecular biology, 350(4), 713-722.

Challenging the Special K Challenge: Especially Convenient or Especially Stupid 14-Day Weight Loss "Solution"?

Image 1: Is this really all it takes to lose those unhealthy and unaesthetic pounds? Two servings of a breakfast cereal a day, instead of two of your regular meals? Sounds too "good" (?) to be true, right? A study says it works, but only the SuppVersity will tell you the real costs!

For me, as a German, it is quite surprising that the words "Special K", or rather the reference to the eponymous product comes up pretty often in the health and nutrition blogosphere, when someone wants to point out an e-special-ly (K) unhealthy breakfast. While "low fat", still looms large here in Germany and "diet"-this and "diet"-that stickers (respective products usually carry the label "light", which shall obviously imply "light" as in "lightweight") are attached to an ever-growing number of products in the mainstream supermarkets, my fellow countrymen (I am unfortunately not so sure about the women, though) must yet have had advanced access to the data (not just the abstract - but more about that later) of Patricia K. Shaw's master thesis (Shaw. 2011), which has been peer-reviewed and published only recently, and are thusly mostly avoiding this "healthy whole grain" product from a company with a >13b revenue in 2010.

"Special K Challenge" - What does it challenge? Weight loss or yo-yo-effect?

In the respective 14-day intervention trial 24 subjects (12 men and 12 women) with a mean age of 34.7 years and a pretty chubby physique (BMI 28.6 kg/m², but body fat 28.8% and 40.7% for men and women, respectively) had to follow the "Special K Challenge" (official website), the central idea of which is that you are going to lose weight and get healthier if you replace two of your regular meals by a predefined amount of yummy (and nutritious *rofl*) expensive cornflakes, ah... I mean "Special K"...

Figure 1: Macronutrient composition of the 174kcal Special  K + skim milk "meal replacement" and the Special K Snack Bars (83kcal) and Mini Breaks (99kcal) the participants consumed during the 14-day challenge and the consequent reductions in protein and fat intake relative to baseline (data calculated based on Shaw. 2011)

In view of the fact that everyone appears to be on the lookout for an easy and above all convenient way to lose weight, it was not difficult for Mrs. Shaw to recruit their subjects among the faculty staff and senior students from the University of Limerick, who actually had to do nothing, but adhere to these two "protocols" for 2x14 days:

1. Control phase: Do what you usually do and eat what you usually eat for two weeks, log all your foods and get back to the lab to get another body weight, body water, body fat, lean body mass (the latter two via DXA scans), waist and hip circumference measurement taken.
    
2. Special K Challenge: Keep doing what you usually do, keep eating what you usually eat, but replace 2 of your main dishes with Special K + semi skimmed milk and eat fruit and/or Special K Mini Breaks or Special K Snack Bars between meals (cf. figure 1), log everything you eat and return your hopefully lighter self as well as the logs to the lab in another two weeks.

About as convenient as the average pizza-ordering slacker likes it, right? It is thusly not really surprising that the overall compliance of 83% was above what you usually see in dietary interventions.

"I want my pizza back!"- and "I better completely stop eating to maximize weight loss"-effect

What is similarly unsurprising, is that the overall calorie intake is reduced (avg. energy deficit: 673kcal/day) by a "challenge" , in the course of which two of the main meals (of which most people obviously consume only three) are replaced with a 174kcal "meal replacement" in form of yummy cornflakes with watery skim milk (aside from the "bah, I want my pizza"-effect, I am thinking about the "hyperpalatability hypothesis" here, as well; cf. Guyenet. 2011). That it is so profoundly reduced that at least one male subject had a caloric deficit of 1555kcal per day (!), however, clearly suggests that the end-result of this type of "diet" (or shall we call it a hunger-strike?) is not going to work. It is thus all the more surprising, that, according to the conclusion of the abstract, ...

The results of the present study demonstrate that the Special K Challenge was effective in reducing total energy intake and resulted in a positive, health-related change in body composition. The reduction in total body mass, regional fat mass and waist circumference may act as an effective motivator to long term body mass reduction.

Certainly worth taking a closer look at the data, right? Well, for the first point, i.e. "effective in reducing total energy intake", we already know that this is true. "Effective", by the way, is effectively understated. Now, what about the "positive, health-related change in body composition"? What would that imply? A reduction in body fat and an increase in lean mass, right! And what have we got?

Figure 2: Lean mass and fat mass of 24 overweight  men and women before 2-week accommodation phase (pre) and before (basal) and after (Special K) 14-day "Special K Challenge" (data adapted from Shaw. 2011)

We got a reduction in body fat and a reduction in lean mass - and worst of all, the female study participants, who, with their 40%+ body fat levels already had no muscle to begin with, lost almost twice as much lean mass as body mass. Assuming that they are "scale watchers" (and should read the "How to track your progress on a diet & exercise regimen"), this may in fact have been an "effective motivator", but it is also a profound obstacle to the "long term body mass reduction", unless we want to define that as "starving your muscles away".

"But it does work! So what do you want?"

Even if you are not effected by it yourself, I bet that everyone of you knows someone who has maybe not even gained weight, but has become fatter and fatter with every diet he (or presumably "she") has "done". This study on the "Special K Challenge" shows you exactly what went wrong for him/her/them:

Image 2: Although common wisdom would say so, eating salad is no alternative either... when I come to think about it, it may be an alternative to eating toilette paper, but that won't help with fat (not just weight!) loss either.

• believing in the existence of a "quick fix" and/or "convenient solution" that will work in 1-2 months, let alone weeks and thusly
• going on a diet instead of changing your diet as part of changing your lifestyle 
• not meeting your minimal energy requirements / starving yourself
• not having enough protein and fat with EVERY meal
• snacking, in general, and on processed foods, in particular
• no exercise (in this case), or tons of endurance exercise to exercise your "cheats" away
• using the scale as a measure of success

Taken together, all that programs failure, no matter how "motivating" it may be... or do you really believe the guy with the -1,500kcal/day deficit or his female counterpart with -1,139kcal/day will "stick" to this "diet" for longer than two weeks? I don't! And we both know what happens, when they are sitting with their friends and family at the coffee, next Sunday, right? ... I guess, it is thus unnecessary that I answer the question I raised in the headline, explicitly - Especially Convenient or Especially Stupid? You decide!